ArticleOncology letters2019
Cervical carcinoma high-expressed long non-coding RNA 1 may promote growth of colon adenocarcinoma through interleukin-17A.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- [IL-17A/lL-17RA reduces cisplatin sensitivity of ovarian cancer SKOV3 cells by regulating autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Study on Clinical Significance of LncRNA EGOT Expression in Colon Cancer and Its Effect on Autophagy of Colon Cancer Cells.Cancer management and research · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical carcinoma high-expressed long non-coding RNA 1 (CCHE1) has been demonstrated to promote several different types of cancer; however, the involvement of CCHE1 in other types of cancer remains unknown. In the present study, the expression levels of CCHE1 and interleukin (IL)-17A were increased in the plasma of patients with metastatic and non-metastatic colon adenocarcinoma (MC and NMC, respectively) compared with the healthy controls. There was no significant difference in the plasma expression levels of CCHE1 and IL-17A in patients with MC compared with patients with NMC. The plasma expression levels of CCHE1 and IL-17A were positively associated with the primary tumor diameter. A significant correlation as demonstrated between the serum levels of CCHE1 and IL-17A in patients with colon adenocarcinoma, but not in the healthy controls. CCHE1 and IL-17A overexpression promoted colon adenocarcinoma cell proliferation. Transfection of small interfering RNA against IL-17A partially reversed the effects of CCHE1 overexpression on cancer cell proliferation. Upregulation of IL-17A was observed after CCHE1 overexpression, while IL-17A overexpression did not significantly change the expression level of CCHE1. Therefore, CCHE1 may promote growth of colon adenocarcinoma through interactions with IL-17A.
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